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Associations between hypobaric hypoxic exposure and urinary leukotriene-E4 (LTE4) were examined in order to determine whether leukotrienes are involved in development of acute mountain sickness (AMS). Eight healthy male volunteers, 19 to 24 years old, were sequentially exposed to the altitude where they normally lived, 50 meters (m) above sea level, to an altitude of 1,830m (moderate altitude (MA)), and an altitude of 4,300m (high altitude (HA)). Exposure to sea level occurred at Natick, Massachusetts. The subjects were then transported by air to Colorado Springs, Colorado for MA exposure. They remained at Colorado Springs for 3.5 days (day) after which they were transported by van to Pikes Peak, Colorado for the HA phase of the experiment where they remained for 4 days. Urine samples were collected at sea level, after 3.5 days at MA, and after 1.5 days at HA. These were analyzed for LTE4. Urinary excretion of LTE4 increased with increasing altitude averaging 67.9 micrograms per milligram creatinine (microg/mg) at sea level, 82.3microg/mg at MA, and 134.8microg/mg at HA. AMS symptoms also increased with increasing altitude. The AMS symptoms at HA were significantly associated with the blood oxygen saturation (SaO2) measured at HA. HA SaO2 was nonsignificantly associated with urinary LTE4 excretion at HA. The authors conclude that urinary LTE4 excretion is elevated upon exposure to HA even after staging at MA for 3.5 days. This is presumed to reflect altitude associated hypobaric hypoxic stress. Urinary LTE4 excretion may correlate with AMS symptoms. Although these findings do not prove that increased production of LTE4 in response to hypoxia causes AMS, given the known activity of LTE4 and similar mediators, it provides more evidence that they are involved in the pathophysiology of AMS.
Chest, 110(4):946-951, 1996. (21 references)
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